Our research aim is to establish Drosophila as a model for Friedreich´s ataxia. This human neurological disorder is produced by the lack of the mitochondrial protein frataxin. Frataxin depletion results in a mitochondrial dysfunction and metabolic problems. We wanted to study wether reduction of frataxin in Drosophila also induced some metabolic responses such as loss of lipid homeostasis. In this work we have found that ubiquitous and glialtargetted reduction of frataxin expression leads to an increase in fatty acids .
 J.A. Navarro et al., Altered lipid metabolismin a Drosophila model of Friedreich s ataxia,Human Molecular Genetics, 2010 1–13doi:10.1093/hmg/ddq183.
Quality and quantity of extracted lipids from Drosophila samples using Precellys®24 technology was sufficient on the one hand to have reliable and reproducible results from different biological replica (not illustrated) and on the other hand to observe clear differences between control flies and frataxindeficient individuals (Figure1). Frataxin deficiency increases the amount of each fatty acid. In conclusion, loss of frataxin affects lipid metabolism and catabolism provoking an accumulation of fatty acids. Moreover, triacylglicerides and other neutral or phospholipids are not so affected.